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首页> 外文期刊>CNS neuroscience & therapeutics. >Resveratrol Protects Vascular Endothelial Cells from High Glucose–Induced Apoptosis through Inhibition of NADPH Oxidase Activation–Driven Oxidative Stress
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Resveratrol Protects Vascular Endothelial Cells from High Glucose–Induced Apoptosis through Inhibition of NADPH Oxidase Activation–Driven Oxidative Stress

机译：白藜芦醇通过抑制NADPH氧化酶激活-驱动氧化应激，保护血管内皮细胞免于高糖诱导的细胞凋亡。

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Summary Introduction Hyperglycemia‐induced oxidative stress has been implicated in diabetic vascular complications in which NADPH oxidase is a major source of reactive oxygen species ( ROS ) generation. Resveratrol is a naturally occurring polyphenol, which has vasoprotective effects in diabetic animal models and inhibits high glucose ( HG )–induced oxidative stress in endothelial cells. Aims We aimed to examine whether HG ‐induced NADPH oxidase activation and ROS production contribute to glucotoxicity to endothelial cells and the effect of resveratrol on glucotoxicity. Results Using a murine brain microvascular endothelial cell line bE nd3, we found that NADPH oxidase inhibitor (apocynin) and resveratrol both inhibited HG ‐induced endothelial cell apoptosis. HG ‐induced elevation of NADPH oxidase activity and production of ROS were inhibited by apocynin, suggesting that HG induces endothelial cell apoptosis through NADPH oxidase–mediated ROS production. Mechanistic studies revealed that HG upregulated NADPH oxidase subunit N ox1 but not N ox2, N ox4, and p22phox expression through NF ‐κB activation, which resulted in elevation of NADPH oxidase activity and consequent ROS production. Resveratrol prevented HG ‐induced endothelial cell apoptosis through inhibiting HG ‐induced NF ‐κB activation, NADPH oxidase activity elevation, and ROS production. Conclusions HG induces endothelial cell apoptosis through NF ‐κB/ NADPH oxidase/ ROS pathway, which was inhibited by resveratrol. Our findings provide new potential therapeutic targets against brain vascular complications of diabetes.
机译：简介简介高血糖症引起的氧化应激与糖尿病性血管并发症有关，其中NADPH氧化酶是产生活性氧（ROS）的主要来源。白藜芦醇是一种天然存在的多酚，在糖尿病动物模型中具有血管保护作用，并抑制高葡萄糖（HG）诱导的内皮细胞氧化应激。目的我们旨在检查HG诱导的NADPH氧化酶激活和ROS产生是否对内皮细胞具有糖毒性，以及白藜芦醇对糖毒性的影响。结果使用鼠脑微血管内皮细胞系bE nd3，我们发现NADPH氧化酶抑制剂（阿波西宁）和白藜芦醇均抑制HG诱导的内皮细胞凋亡。载脂蛋白抑制了HG诱导的NADPH氧化酶活性的升高和ROS的产生，这表明HG通过NADPH氧化酶介导的ROS的产生诱导内皮细胞凋亡。机理研究表明，HG通过NFκB激活上调了NADPH氧化酶亚基N ox1，但没有上调N ox2，N ox4和p22phox的表达，这导致NADPH氧化酶活性升高并由此产生ROS。白藜芦醇通过抑制HG诱导的NFκB活化，NADPH氧化酶活性升高和ROS产生来预防HG诱导的内皮细胞凋亡。结论HG通过白藜芦醇抑制NF-κB/ NADPH氧化酶/ ROS途径诱导内皮细胞凋亡。我们的发现为糖尿病的脑血管并发症提供了新的潜在治疗靶标。

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